TRAIL‐Induced Apoptosis

Corazza, Nadia; Kassahn, Daniela; Jakob, Sabine; Badmann, Anastasia; Brunner, Thomas

doi:10.1111/j.1749-6632.2009.04905.x

Cited by 41 publications

(25 citation statements)

References 59 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This change recruits cytoplasmic adaptor proteins (such as Fas-associated protein with death domain [FADD]), and the latter recruits apoptosis signaling molecules (such as caspase-8). The DR, adaptor protein, and associated apoptosis signaling molecule form the death-inducing signaling complex (DISC), thus leading to the activation of the effector caspase cascade (which typically involves caspase-3, -6, and -7) 8–10. Cellular FADD-like interleukin-1β (IL-1β) converting enzyme inhibitory protein (c-FLIP) can inhibit DISC and prevent apoptosis 11…”

Section: Hepatocyte Apoptotic Pathwaysmentioning

confidence: 99%

See 1 more Smart Citation

Mechanism of Hepatocyte Apoptosis

et al. 2016

View full text Add to dashboard Cite

Hepatocyte apoptosis plays important roles in both the removal of external microorganisms and the occurrence and development of liver diseases. Different conditions, such as virus infection, fatty liver disease, hepatic ischemia reperfusion, and drug-induced liver injury, are accompanied by hepatocyte apoptosis. This review summarizes recent research on the mechanism of hepatocyte apoptosis involving the classical extrinsic and intrinsic apoptotic pathways, endoplasmic reticulum stress, and oxidative stress-induced apoptosis. We emphasized the major causes of apoptosis according to the characteristics of different liver diseases. Several concerns regarding future research and clinical application are also raised.

show abstract

Section: Hepatocyte Apoptotic Pathwaysmentioning

confidence: 99%

“…In hepatocytes, the apoptotic signals from DR are typically not powerful enough to initiate the effector caspase cascade, so the mitochondria-mediated pathway is generally used to amplify it 8,10. This amplification is extremely important for TNF-α-mediated hepatocyte apoptosis 16.…”

Section: Hepatocyte Apoptotic Pathwaysmentioning

confidence: 99%

Mechanism of Hepatocyte Apoptosis

et al. 2016

View full text Add to dashboard Cite

show abstract

“…For this reason, TRAIL has recently received much attention because it preferentially kills tumor cells while leaving normal cells unaffected. However, a considerable number of tumors are resistant to TRAIL-induced apoptosis [17,21]. Various conventional chemotherapeutic agents have been demonstrated to synergistically augment TRAIL-induced apoptosis through induction of DR5 expression.…”

Section: Discussionmentioning

confidence: 99%

“…In particular, TRAIL is considered as the most promising anticancer agent in the TNF superfamily because of its selective cytotoxicity against tumor cells versus normal primary cells. TRAIL induces apoptosis in various cancer cells through its interaction with death receptor 5 (DR5), which contains a cytoplasmic death domain capable of recruiting apoptosis signaling molecules and inducing apoptosis [15-21]. However, many tumor cells are resistant to TRAIL-induced apoptosis [22,23].…”

Section: Introductionmentioning

confidence: 99%

5-allyl-7-gen-difluoromethoxychrysin enhances TRAIL-induced apoptosis in human lung carcinoma A549 cells

et al. 2011

View full text Add to dashboard Cite

Background5-allyl-7-gen-difluoromethoxychrysin (AFMC) is a novel synthetic analogue of chrysin that has been reported to inhibit proliferation in various cancer cell lines. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a promising anti-cancer agent.MethodsThe cytotoxicity of A549 and WI-38 cells were determined using colorimetry. Apoptosis was detected by flow cytometry (FCM) after propidium iodide (PI) fluorescence staining and agarose gel electrophoresis. Caspase activities were evaluated using enzyme-linked immunosorbent assay (ELISA).The expressions of DR4 and DR5 were analyzed using FCM and western blot.ResultsSubtoxic concentrations of AFMC sensitize human non-small cell lung cancer (NSCLC) A549 cells to TRAIL-mediated apoptosis. Combined treatment of A549 cells with AFMC and TRAIL significantly activated caspase-3, -8 and -9. The caspase-3 inhibitor zDEVD-fmk and the caspase-8 inhibitor zIETD-fmk blocked the apoptosis of A549 cells induced by co-treatment with AFMC and TRAIL. In addition, we found that treatment of A549 cells with AFMC significantly induced the expression of death receptor 5 (DR5). AFMC-mediated sensitization of A549 cells to TRAIL was efficiently reduced by administration of a blocking antibody or small interfering RNAs against DR5. AFMC also caused increase of the Sub-G1 cells by TRAIL treatment and increased the expression levels of DR5 in other NSCLC H460 and H157 cell lines. In contrast, AFMC-mediated induction of DR5 expression was not observed in human embryo lung WI-38 cells, and AFMC did not sensitize WI-38 cells to TRAIL-induced apoptosis.ConclusionsAFMC synergistically enhances TRAIL-mediated apoptosis in NSCLC cells through up-regulating DR5 expression.

show abstract

“…Nonetheless, the putative role of these polymorphisms in disease susceptibility has been examined in genetic association studies of various inflammatory disorders, including Crohn's disease [10-13], ulcerative colitis [10,11,14], systemic lupus erythematosus [15-17] and rheumatoid arthritis [18,19]. More recently, given that cancer progression is preceded by a long period of subclinical inflammation [20-22], the genetic polymorphisms of TNF-α , TNFRSF1A and TNFRSF1B have been examined in terms of susceptibility to various cancers [23-28]. In this study, genetic polymorphisms of the TNFRSF1B gene, M196R/T587G, A1466G and C1493T, were evaluated in Japanese ESCC patients treated with a definitive 5-FU/CDDP-based chemoradiotherapy, and their predictive values of prognosis or severe acute toxicities were assessed.…”

Section: Introductionmentioning

confidence: 99%

TNFRSF1B A1466G genotype is predictive of clinical efficacy after treatment with a definitive 5-fluorouracil/cisplatin-based chemoradiotherapy in Japanese patients with esophageal squamous cell carcinoma

Kuwahara

Yamamori

Fujita

et al. 2010

J Exp Clin Cancer Res

View full text Add to dashboard Cite

BackgroundCurrently definitive 5-fluorouracil (5-FU)/cisplatin (CDDP) -based chemotherapy is recognized as one of the most promising treatments for esophageal cancer. A series of studies performed found genetic polymorphisms and the plasma concentration of 5-FU to be predictive of acute severe toxicities and clinical response. Genetic polymorphisms of tumor necrosis factor (TNF) -α and its surface receptors, TNFRSF1A and TNFRSF1B have been examined in terms of susceptibility to various cancers. In this study, genetic polymorphisms of TNFRSF1B gene were evaluated Japanese esophageal squamous cell carcinoma (ESCC) patients treated with the definitive 5-FU/CDDP-based chemoradiotherapy and their predictive values of prognosis or severe acute toxicities were assessed.MethodsForty-six patients with ESCC were treated with the definitive 5-FU/CDDP-based chemoradiotherapy, one course of which consisted of the continuous infusion of 5-FU for days 1-5 and 8-12, the infusion of CDDP on days 1 and 8, and the radiation at 2 Gy/day on days 1-5, 8-12, and 15-19, with a second course repeated after 2-week interval. Genetic polymorphisms of a TNF-α receptor TNFRSF1B gene were determined by a TaqMan® MGB probe-based polymerase chain reaction.ResultsThe genotype of TNFSR1B A1466G, but not M196R/T587G or C1493T, was found to be predictive of clinical response, i.e., a complete response or not (p = 0.040). Clinical response was predicted by tumor size (p = 0,002), lymph node metastasis (p = 0.007), distant metastasis (p = 0.001) and disease stage (p < 0.001), but TNFRSF1B A1466G genotype was independent of these factors.ConclusionsGenetic polymorphism of TNFRSF1B A1466G was found to be predictive response in Japanese ESCC patients with a definitive 5-FU/CDDP-based chemoradiotherapy. Further clinical investigation with a large number of patients or experiments in vitro should be performed to assess the predictive value of TNFRSF1B A1466G genotype after chemoradiotherapy.

show abstract

TRAIL‐Induced Apoptosis

Cited by 41 publications

References 59 publications

Mechanism of Hepatocyte Apoptosis

Mechanism of Hepatocyte Apoptosis

5-allyl-7-gen-difluoromethoxychrysin enhances TRAIL-induced apoptosis in human lung carcinoma A549 cells

TNFRSF1B A1466G genotype is predictive of clinical efficacy after treatment with a definitive 5-fluorouracil/cisplatin-based chemoradiotherapy in Japanese patients with esophageal squamous cell carcinoma

Contact Info

Product

Resources

About